Tamoxifen affects the histology and hepatopancreatic lipid metabolism of swimming crab Portunus trituberculatus.

• The effect of tamoxifen on lipid metabolism of Portunus trituberculatus was investigated. • Tamoxifen up-regulated the expression level of carnitine palmitoyltransferase I. • The lowest levels of free fatty acids were detected in 20 μg g−1 TAM treatments. • Tamoxifen caused the walls of the hepatopancreatic tubules to become brittle. Tamoxifen (TAM) is an antiestrogenic agent and can enter the aquatic environment in wastewater. It has been reported that TAM can induce hepatic steatosis in vertebrates, however, the effects of TAM exposure on lipid metabolism of hepatopancreas in crustaceans remains unclear. In this study, four TAM concentrations (0, 6.7, 13.4 and 20 μg g−1 crab body weight) were injected into the swimming-leg of swimming crabs Portunus trituberculatus , as a means of evaluating the effects of TAM on the expression levels of lipid metabolism-related genes, lipid composition, and hepatopancreas histology. The results showed that the mRNA levels of three lipogenic related genes (diacylglycerol acyltransferase 1 (DGAT1), acetyl-CoA carboxylase (ACC) and fatty acyl desaturase (FAD)) decreased significantly in the 6.7 μg g−1 and 20 μg g−1 TAM treatments compare to the control. The mRNA levels of fatty acid synthase (FAS) decreased significantly in a dose-dependent manner as TAM concentration increased. The mRNA levels of two lipid catabolism-related genes (acyl-CoA oxidase (ACOX) and fatty acid transport protein (FATP)) were down-regulated among the three TAM treatments, while the enzyme activity and mRNA level of carnitine palmitoyltransferase I (CPT-I) was up-regulated by TAM treatments. Compared to the control, the lowest levels of total lipids and phospholipids were detected in the 6.7 μg g−1 TAM treatment, while the 20 μg g−1 TAM treatment had the lowest free fatty acids concentration. The 6.7 μg g−1 TAM treatment had the lowest percentages of 16:1n-7, 18:1n-9, 18:1n-7 and total monounsaturated fatty acids (∑MUFA), whilst simultaneously recording the highest percentages of 18:2n-6 and 20:2n-6 in this treatment. Moreover, histological observations indicated that TAM caused the walls of the hepatopancreatic tubules to become brittle, with a concurrent increase in the number of blister-like cells. These results suggest that TAM damages the hepatopancreas and leads to a reduction in hepatopancreatic lipid deposition in P. trituberculatus. [ABSTRACT FROM AUTHOR]